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General Medicine sara > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Describe where the pituitary gland is found

A

In the pituitary fossa/ sella turcica which is part of the sphenoid bone at the base of the skull

It lies below the hypothalamus and is connected to the hypothalamus by a stalk

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2
Q

What is the composition of the pituitary ?

A

Made up of the anterior pituitary (2/3 - adenohypophysis) and posterior pituitary (1/3- neurohypophysis)

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3
Q

What is the pituitary derived from?

A

Anterior pituitary from the oral ectoderm (Rathke’s pouch) - therefore glandular
Posterior pituitary from the diencephalon - outgrowth of hypothalamus - therefore neuronal

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4
Q

How is the pituitary connected to the hypothalamus?

A

Anterior by a collection of blood vessels which forms a portal system - superior hypophyseal arteries

Posterior by neurons

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5
Q

Name some structures that are anatomically close to the pituitary .

A

Optic chiasm - superior
Sphenoid sinus - inferior
Cavernous sinus (including ICA, CN III, IV, VI and V) - lateral

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6
Q

Name 5 cells making up the anterior pituitary and state the hormone they release

A

Thyrotropes - thyroid stimulating hormone
Corticotropes - adenocorticotrohin hormone (ACTH)
Gonadotropes - LH and FSH
Somatotropes - GH
Lactotropes - prolactin

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7
Q

Name hormones that influence GH release

A

Stimulated by GHRH

Inhibited by IGF1 and somatostatin

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8
Q

Name hormones that influence the release of prolactin

A

Stimulated by TRH and oestrogen

Inhibited by dopamine

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9
Q

Name hormones that influence the release of FSH and LH

A

Stimulate - GnRH

Inhibit- oestrogen , progesterone, inhibin

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10
Q

Name hormones that influence the release of TSH?

A

Stimulated by TRH

Inhibited by somatostatin, T4/3

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11
Q

Name hormones that influence ACTH release

A

Stimulated by CRH

Inhibited by cortisol

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12
Q

Name two hormones released by the posterior pituitary and where are these made?

A

Oxytocin and ADH

Made by hypothalamic neurons

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13
Q

How are basal and dynamic tests used for pituitary hormone deficiency?

A

Basal test:

  • measure the basal level of pituitary hormone (e.g. TSH) and target hormone (T4)
  • if these are both low suggestive of pituitary deficiency

Dynamic test:
- next you would stimulate the pituitary to access the reserve

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14
Q

How can basal and dynamic tests be used for pituitary hormone excess?

A

Basal:
Measure basal level of pituitary hormone and its target - if there is pituitary hormone excess they will both be high

Dynamic
- suppression test to assess if the pituitary is in hypersecretory state

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15
Q

What is the basal test for gonadotropes?

A

Test the levels of FSH, LH and testosterone and oestrogen

In premenopausal women do this 1-5 days after the menstrual cycle to avoid variance throughout cycle

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16
Q

What is the dynamic test for gonadotropes ?

A

GnRH testing

Used to assess pubertal disorder e.g. Precocious puberty

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17
Q

How do we test somatotropes with basal testing?

A

Test GH and IGF1 levels
However IGF1 is not a good indicator of GH deficiency in +40yrs
GH is only a good indicator if very low or high

However if IGF1 is low in combination to low levels of 3 other pituitary hormones , it is a good indicator of GH deficiency

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18
Q

Describe the suppression test for acromegaly

A

Glucose inhibits GH release
Therefore glucose is given after an overnight starve
GH is measured every 30 mins for 2 hours
Normally GH is suppressed to <1mcg/dL. Otherwise suggestive of excess GH

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19
Q

Describe the stimulation test for GH

A

INsulin tolerance test is used
Insulin is given which causes hypoglycaemia which is a stimulant for GH release

GH will normally rise in response to this. If it doesn’t there is a problem in pituitary

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20
Q

How is basal testing used to test the corticotropes?

A

Measure cortisol level in serum or saliva
Should be between 3-18 mcg/dL

In morning cortisol is highest and therefore if levels are lower than 3 suggestive of deficiency

In night cortisol is lowest and so if levels are higher than 18 suggestive of excess

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21
Q

Name 4 corticotropes stimulation tests

A

Insulin tolerance test - gold standard
Metyrapone - gold standard
Synacthen test
CRH test

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22
Q

Describe the insulin tolerance test for corticotrope function

A

Insulin is given which leads to hypoglycaemia and normally this results in cortisol release

The aim is to get glucose below 40mg/dL which should lead to cortisol of more than 18

If cortisol doesn’t reach this level , it indicates adrenal insufficiency

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23
Q

What is the problem with the insulin tolerance test and what are the contraindications ?

A

Problem: labour intensive because needs close monitoring

Contraindications :

- elderly
- seizures
- abnormal ECG
- ischaemic heart disease
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24
Q

Describe the metyrapone test

A

Metyrapone inhibits b hydroxylation in the adrenal cortex and thus 11 hydroxycortisol is not converted into cortisol

In a normal person we would expect cortisol levels to drop, ACTH to rise and 11 hydroxycortisol to rise

If both ACTH and 11 hydroxycortisol do not rise : problem with hypothalamus / pituitary

If ACTH rises but not 11-hydroxycortisol then there is adrenal insufficiency

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25
Q

What is the problem with the metyrapone test?

A

Reduced responses can also be seen in:
Thyrotoxicosis
Pregnancy
Oral contraceptives / phenytoin

So may get false positive results

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26
Q

Describe the synacthen test

A

Measure basal cortisol levels
Synthetic ACTH given
Measure cortisol 30 mins and 1 hour after

Normal : cortisol should double
If there is adrenal insufficiency it will remain low

(Results will be unreliable if there is a problem with pituitary/hypothalamus)

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27
Q

Describe the CRH test

A

IV CRH is given which leads to increased ACTH and cortisol after 15/30 mins

The rise is more prominent in those with cushings

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28
Q

Name 2 suppression tests for corticotropes

A

1mg dexamethasone suppression

8mg dexamethasone suppression

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29
Q

What is the 1mg dexamethasone suppression test

A

1mg of dexamethasone is given between 11pm and 12 pm at night and then cortisol is measured in the morning

If cortisol is suppressed less than 1.8mcg/dL then this excludes cushings

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30
Q

What is the 8mg dexamethasone suppression test ?

A

8mg of dexamethasone is given at night and cortisol is measured in the morning

If cortisol drops less than 50% it indicates cushings disease
If cortisol doesn’t drop this much it is suggestive of ectopic ACTH secretion

This is performed after 1mg dexamethasone suppression when cushings is diagnosed and you want to distinguish between whether it is from pituitary or ectopic

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31
Q

How are lactotropes and thyrotropes tested ?

A

Lactotropes basal test: fasting PRL levels
Thyrotropes Basal test: TSH , t4 and t3

No functional tests for either

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32
Q

How are pituitary tumours classified?

A

Microadenoma: <1cm
Macroadenoma : >1cm

Non functioning : gonadotropinomas
Functioning: prolactinoma (most common), acromegaly, cushings, TSH adenoma (rare)

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33
Q

How are non functioning microadenomas treated?

A

Reassess periodically

No indication for surgery unless they are functional or have mass effects

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34
Q

How are non functional macroadenomas treated

A

If they have mass effects then surgery is indicated (transsphenoidal surgery)

Otherwise reassess periodically

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35
Q

What is the first line treatment for functioning pituitary adenomas?

A

Prolactinoma - dopamine agonist

For all others first line is TSS

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36
Q

Describe the tumour mass effects of pituitary adenomas (macroadenomas)

A 
Headaches
Hypopituitarism 
Visual field defects
Visual loss - optic nerve atrophy 
Opthalmoplegia / CN palsy - III, IV,VI
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37
Q

If a pituitary adenomas is suspected what are the generalised investigations that should be carried out?

A

Basal and dynamic hormone tests

Visual field testing

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38
Q

Who do prolactinoma mainly occur in?

A

Women

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39
Q

What are the effects of prolactinoma s

A

Effects of hyperprolactinaemia: galactorrhoea, hypogonadotophic hypogonadism (prolactin inhibits GnRH), amenorrhoea , reduced labido/fertility and reduced bone density

Mass effects of tumour

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40
Q

How are prolactinoma treated?

A

Dopamine agonsit - cabergoline (first line)
Surgery - TSS (if resistant or intolerant to above )
Radiotherapy for recurrent prolactinoma

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41
Q

What is transphenoidal surgery

A

Instruments (endoscopy and surgical equipment) are passed up the nose

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42
Q

What are the causes of hyperprolactinaemia

A

Pregnancy

Prolactinoma, meningioma and glioma
Head injury/ surgery
Primary hypothyroid ( increased TSH which stimulates PRL)
Drugs : dopamine antagonist (metaclopramide) , neuroleptics, antidep, methyl dopa, opioids
CKD - reduced clearance

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43
Q

What are the causes of acromegaly?

A

Excess GH due to

Mainly due to pituitary tumour but can be due to hypothalamic tumour and ectopic GnRH from carcinoid tumour

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44
Q

What are the complications of acromegaly

A 
Hypertension 
Diabetes
Cvs disease (arrhythmia and valve disease)
Increased risk of colon cancer 
Vertebral fractures
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45
Q

What are the clinical features of acromegaly?

A

Msk: carpal tunnel, arthralgia , muscle weakness
Facial: prognathism (lower jaw protrudes ), frontal bossing (big forehead), course features (large tongue and nose)
Deep voice, sweating, tired
Large hands and feet
Mass tumour effects

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46
Q

What investigations should be carried out if acromegaly is suspected ?

A

Basal GH and IGF1 levels matched for age and gender
Oral glucose tolerance test is indicated if symptoms of acromegaly but IGF1 is normal (this is suppression test for acromegaly)

If either of above are abnormal do MRI

Check visual fields, blood pressure, urinalysis and other hormones

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47
Q

How is acromegaly managed?

A

If pituitary tumour is found then TSS
Radiotherapy
Somatostatin analogue (octreotide )
GH receptor blocker (pegvisomant )

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48
Q

How is cushings diagnosed ?

A

Dynamic and basal testing
E.g. 24 hour urinary cortisol (basal test)

MRI of brain

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49
Q

How can cushings disease be treated ?

A

TSS - first line
Medical:
- metyrapone : hydroxylation antagonist (11 b hydroxylase)
- ketoconazole : indicated in children

Radiotherapy

Need to follow up after treatment to ensure no adrenal insufficiency

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50
Q

What are the side effects of metyrapone and ketoconazole?

A

Metyrapone: nausea, reduced BP and neutropenia

Ketoconazole : abnormal liver function and gynacomastia

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51
Q

How do thyrotrophinomas present clinically

A

Same as hyperthyroid and goitre

However most are macroadenomas when diagnosed and so often mass effects of tumour are experienced too

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52
Q

How are thyrotrophinomas managed?

A

TSS - first line
Somatostatin analogues ( octreotide )
B blockers for other symptoms
Radiotherapy if everything fails

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53
Q

What are the differentials for high TSH and high T4/3

A

TSH secreting tumour

Thyroid hormone resistance

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54
Q

What is the most common non functioning pituitary tumour

A

Gonadotropinoma

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55
Q

How do gonadotrophinomas normally present

A

Because they are usually non functioning tumours they mainly present as mass effects of tumour rather than GnRH excess (precocious puberty and testicular enlargement )

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56
Q

What investigations should you do if you investigate a gonadotrophinoma

A

Imaging - MRI or CT
Visual field assessment
May have mild prolactinoma due to stalk compression

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57
Q

How do you manage a gonadotrophinoma

A

TSS
Radiotherapy if tumour is invasive / recurrent
- risk of hypopituitarism

Dopamine agonists, somatostatin analogues and GnRH antagonist / agonist

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58
Q

What is hypopituitarism

A

Partial or complete deficiency of one or more pituitary hormones

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59
Q

What are the causes of hypopituitarism

A

Trauma
Infection - TB, meningitis , pituitary abscess
Radiotherapy due to tumour of pituitary or hypothalamus
Parasellar tumours- meningioma and gliomas
Infiltration disease - haemochromatosis and sarcoidosis
Isolated hypothalamic releasing hormone deficiency - Kallmans syndrome - congenital GnRH deficiency and anosmia

Apoplexy and empty sella syndrome

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60
Q

What is apoplexy?

A

Caused by infarction to pituitary
Occurs in 10-15 % of pituitary adenomas

Sudden headache, visual impairment , opthalmoplegia (paralysis / weakness of eye muscles) and altered mental state

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61
Q

What is empty sella syndrome ?

A

Sella is filled with CSF
Can occur secondary to removal of tumour
Therefore associated with hypopituitarism

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62
Q

List the order of hormone deficiencies seen most commonly to least commonly in hypopituitarism

A

GH, GnRH - most common
ACTH and TSH
PRL
ADH - deficiency is very rare in pituitary adenomas

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63
Q

What investigations would you carry out in hypopituitarism

A

Basal and dynamic function tests
Test posterior pituitary by: serum sodium, serum osmolality, urine osmolality and urine volume in 24 hours

Water deprivation test if suspected diabetes insipidus

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64
Q

What are the feature of reduced GH in children and adults ?

A

Children: short stature and reduced bone/ muscle maturation

Adults: increased central fat, reduced muscle mass, reduced exercise capacity, increased CVS risk, tired

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65
Q

What are the features of reduced LH,FSH in children, women and men

A

Children : delayed puberty
Men: testicular atrophy, reduced libido, reduced muscle mass , erectile dysfunction
Women: breast atrophy, anovulation , vaginal dryness, hot flush

Both: reduced fertility and bone mineral density

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66
Q

What are the features of low ACTH

A

Addison’s disease features

But no hyperpigmentation or hyperkalaemia

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67
Q

What is seen if prolactin is deficient

A

No lactation

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68
Q

How are hypopituitarism treated ?

A

Treat cause
Hormone replacement
- e.g. Glucocorticoids replacement if ACTH deficiency - prednisolone or hydrocortisone. The aim is to aim for the lowest dose possible to eliminate symptoms and avoid symptoms of excess

  • GH replacement
  • thyroid hormone replacement - give thyroxine and monitor treatment using T4 levels
  • sex hormone replacement
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69
Q

How is GH replacement achieved

A

GH given depending on age
Start low and titrate according to clinical response, IGF1 levels and side effects

Annual lipid levels , fasting blood sugar and DXA scan

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70
Q

What is the problem with GH replacement

A

Reversible dose dependant side effects :
Carpal tunnel , headaches, peripheral oedema, hypertension and diabetes

GH increases metabolism of TSH and cortisol and so starting GH replacement can unmask subclinical adrenal / thyroid insufficiency

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71
Q

Where are the adrenals found ?

A

Superior pole of kidneys

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72
Q

State the different parts of the adrenal and what they secrete

A

Adrenal medulla and cortex (different embryological origins )

Medulla:

  • sympathetic neurons without axons
  • these are controlled by presynaptic sympathetic neurons
  • release adrenaline and noradrenaline

Cortex:

  • inner zone: zona reticularis - secrete androgens DHEA (also glucocorticoids )
  • middle zone: zona fasciculata - secrete glucocorticoids
  • outer zone: zona glomerulosa - secrete mineralocorticoids
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73
Q

Why is cortisol needed for the adrenal medulla

A

Converts NA to adrenaline

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74
Q

Where do the adrenal veins empty and where do the lymphatics drain ?

A

Left adrenal vein into left renal vein
Right adrenal vein into IVC

Paraaortic nodes

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75
Q

what stimulates and what is the action of the mineralocorticoids?

A

stimulated by ACTH, angiotensin II and high K (however ACTH is not that important, mainly for cortisol and therefore if deficient doesn’t affect aldosterone much)
aldosterone acts on DCT and collecting duct –> increase gene expression of ENaC, ROMK, Na/K ATPas and Na/H. Therefore increases sodium and water retention to increase blood volume and blood pressure

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76
Q

what is the action of glucocorticoids

A

regulate metabolism of carbohydrates and fats.
immunosuppressive and anti inflame
regulate stress response

act on gene expression e.g. inhibit expression of phospholipase II and therefore prostaglandin production

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77
Q

how is cortisol release controlled? how does cortisol travel in plasma?

A

CRH –> POMC –> POMC is cleaved to give ACTH which acts on GPCR to stimulate cortisol release
cortisol levels are highest in the morning

travels in plasma bound to cortisol binding protein and albumin and so small amount is free

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78
Q

what androgens do the adrenals produce and is this a significant amount? Are these strong?

A

DHEA and Androstendione
small proportion of total body androgen
weak but converted into stronger form by peripheral aromatase enzyme

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79
Q

how does cushings affect carbohydrate, protein and fat metabolism

A

carbohydrate: increases gluconeogenesis and reduces glucose uptake. Therefore leads to glucose intolerance and predisposes to diabetes
protein: increases breakdown of protein. muscle wasting, thin arms and legs, thin skin and brusing
fat: stimulates lipolysis and increases free fatty acid levels. Fat redistributes to the abdomen (trunkal obesity), to the face (moon face), to the back of the neck (buffalo hump)

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80
Q

what is cushings

A

syndrome of glucocorticoid excess and the symptoms accompanying this.
usually occurs gradually

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81
Q

how does cushings affect the immune system and endocrine system?

A

immune system: inhibition of immune cells. inhibits cytokine and Ab production therefore more prone to infections and poor healing.

endocrine: supresses other hormones of anterior pituitary –> delayed growth in children

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82
Q

how does cushings affect the nervous system?

A

influences foetal neuronal development
changes behaviour and cognition

insomnia, psychosis, depression and confusion

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83
Q

how does cushings affect water and calcium metabolism?

A

water: has mild mineralocorticoid action and thus can result in water and sodium retention. hyper Na and hypertension. (note often hyperaldosteronism accompanies cushings and adds to these symptoms)

reduced calcium absorption from the gut and increased calcium excretion from kidneys. promotes bone breakdown. results in osteoporosis, fractures, vertebral collapse and kyphosis

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84
Q

list the symptoms/clinical features of cushings

A

face: moon face, acne, cataracts, hirsutism, male pattern of baldness
brain: depression, confusion, psychosis, insomnia
adipose: buffalo hump, trunkal obesity
skin: straie, brusing, poor healing, sometimes increased pigmentation (cushings disease), ankle oedema
muscle: wasting so thin arms and legs
abdomen: renal stones and peptic ulcers
heart: predisposed to congestive heart disease, hypertension
bones: osteoporosis, fractures and kyphosis
blood: hyperglycaemia and possible diabetes

a lot of symptoms of cushings can be seen anyway. the most indicative are muscle wasting, bruising, red face and stretch marks.

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85
Q

How is cushings diagnosed by investigations?

A

24 urinary cortisol measurement
1mg dexamethasone test - if this does not supress <1.8mg then classified as cushings
further investigations can determine if cushings disease or ectopic:
- 8mg dexamethasone test - if supressed, then likely to be disease. if not supressed likely to be ectopic secretion
- CRH test - cortisol will increase if pituitary but not really change if ectopic.

check BP and glucose

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86
Q

what is pseudocushings?

A

some conditions (obesity, depression, alcohol) will lead to increased metabolism of dexamethasone and thus dexamethasone will not supress cortisol and cushings can be diagnosed when really there is no cushing

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87
Q

what are the causes of cushings?

A

exogenous: steroid use
disease: pituitary oversecretion of ACTH e.g. adenoma
ectopic ACTH: anaplastic small cell lung cancer, pancreatic, ovarian and thymus tumours, carcinoid tumour
adrenal: adrenal hyperplasia, tumour, carcinoma

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88
Q

what signs are suggestive of cushings disease rather than cushings syndrome?

A

bilateral adrenal hyperplasia (ACTH will be causing both adrenals to enlarge)

hyperpigmentation due to POMC cleaving to give ACTH and a-MSH

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89
Q

How is subclinical cushings characterised? is subclincal cushings a problem?

A

normal urinary cortisol levels
failure to supress cortisol after 1mg dexamethasone

yes because at risk of diabetes, hypertension and osteoporosis

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90
Q

what is meant by plethoric ?

A

A word to describe someone looking swollen, fat, overfull. often used to describe faces in cushings syndrome

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91
Q

what are the symptoms of mineralocorticoid excess?

A

hypertension (H20 and Na retention)
hypokalaemia (muscle spasms and weakness)
alkalosis (increased expression of Na/H)
polyuria and polydipsia (reduced ability to concentrate)
headaches and lethargy

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92
Q

what is the difference between primary and secondary mineralocorticoid excess?

A

primary: autonomous aldosterone hypersecretion i.e. renin is low
secondary: aldosterone is high because renin is high

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93
Q

what are the causes of primary mineralocorticoid excess?

A

conns
bilateral adrenal hyperplasia
aldosterone producing adrenal carcinoma

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94
Q

what are the causes of secondary mineralocorticoid excess?

A 
liver cirrhosis
heart failure
renal artery stenosis
nephrotic syndrome
renin producing tumour (RARE)
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95
Q

who is Conns most likely to affect?

A

women in 3rd -6th decade

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96
Q

What is more likely to be the cause of hyperaldosteronism.. conns or bilateral adrenal hyperplasia?

A

bilateral adrenal hyperplasia is more common

but usually occurs later in life than Conns

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97
Q

what investigations would you want to carry out if you suspect mineralocorticoid excess?

A

blood tests: looking for hypernatraemia, hypokalaemia, raised aldosterone.
- Is renin high or low? look at aldosterone:renin ratio - to tell you if primary or secondary

Blood pressure - hypertensive
CT/MRI of adrenals
ECG due to electrolyte disturbances

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98
Q

what is a pheochromocytoma?

A

An adrenomedullary catecholamine secreting tumour

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99
Q

why are pheochromocytomas important to look for even though they are usually rare?

A

Can cause potentially fatal hypertensive crisis

very easily cured by surgery and do not need life long medication

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100
Q

what conditions are associated with pheochromocytomas?

A

neurofibromatosis (autosomal dominant)
familial carotid body tumours
MEN IIa and IIb

sporadic pheochromocytomas are usually unilateral but if associated with another condition they are often bilateral

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101
Q

what are the clinical features of pheochromocytomas?

A 
tachycardia, palpitations, chest pain 
dyspnoea 
Anxiety
pallor/flushings, sweating , nausea
headaches and pyrexia 
raised BP
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102
Q

who should be screened for a pheochromocytoma?

A

family history
young and hypertensive
unexplained heart failure
adrenal incidentaloma

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103
Q

what are the complications of pheochromocytomas?

A

CVS strain –> left ventricular failure/ arrhythmias

lungs: pulmonary oedema
metabolism: carb intolerance, raised Ca
neuro: cerebrovascular hypertension and encephalopathy

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104
Q

what investigations can be carried out if you suspect a pheochromocytoma?

A

urinary catecholamine concentration

metaadrenalines in urine/plasma - more specific

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105
Q

what treatment can be used for pheochromocytomas?

A 
alpha blockade = phenoxybenzamine 
  - important that these are started before B blockers
Then start propranolol 
eventually.. 
surgical resection - curative

need to have check ups of urinary catecholamines and BP

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106
Q

what is congenital adrenal hyperplasia (CAH)? (include cause and consequences)

A

deficiency in 21 hydroxylase enzyme (responsible for making aldosterone and cortisol)
Therefore ACTH rises (lack of negative feedback)
ACTH causes adrenal hyperplasia

lack of aldosterone –> salt loosing crisis and neonatal shock

large adrenals produce excess androgens –> precocious puberty and pseudopuberty (secondary characteristics at 6 months) and masculinisation in females

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107
Q

name 3 medications affecting adrenal hormone production?

A

phenytoin, ketonazole and fluconazole

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108
Q

what is the difference between primary and secondary adrenal insufficiency?

A

primary - adrenals themselves are the problem. usually affects all 3 layers and get deficiencies in all 3 hormones. e.g. CAH and addisons . ACTH can be high leading to pigmentation.

secondary: the problem is in the pituitary or hypothalamus, less ACTH. In this case the main effect is lack of cortisol because there are other stimulants for aldosterone release. Also no pigmentation. May have other problems e.g. visual field defects, headaches.

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109
Q

what are the causes of secondary adrenal insufficiency ?

A

anything affecting the pituitary: sarcoidosis, TB, adenoma, haemochromatosis

suppression by exogenous steroids

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110
Q

why should steroids never be abruptly stopped?

A

exogenous steroids will supress the HPA in long run and thus if suddenly stopped the pituitary needs time to adapt and if this time is not given , addisons disease can result.

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111
Q

who is addisons disease more common in ?

A

women

(autoimmune diseases are more common in women.

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112
Q

what is addisons disease?

A

primary insufficiency of adrenal cortex characterised by mineralocorticoid and glucocorticoid deficiencies.

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113
Q

what is the cause of addisons disease?

A

progressive destruction of the adrenal cortex caused by:

  • autoimmune destruction (most common)
  • infection (TB)
  • haemochromatosis
  • metastasis (lung, breast, kidney and lymphoma)
  • haemorrhage
  • adrenalectomy
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114
Q

what are the clinical features of addisons disease?

A

general: malaise, low grade fever, tired, weak, anorexia, weight loss
GI: abdo pain, diarrhoea, vomiting and nausea
Pigmentation around nipples, armpits and creases of hands.
dizziness and postural hypotension
arthralgia and myalgia

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115
Q

what is addisonian crisis?

A

sudden onset of symptoms of addisons as levels of cortisol suddenly drop

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116
Q

what are the symptoms of addisonian crisis?

A 
abdo pain, nausea and vomiting
back pain 
hypotension and shock 
unexplained fever
lack of fluid
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117
Q

what may trigger addisonian crisis?

A

infection
stress
surgery (why it is important to continue steroids)

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118
Q

how do you treat addisonian crisis?

A 
IV  0.9% saline  
glucose
hydrocortisone IV 
monitor U&amp;E and glucose 
catheterise for fluid balance
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119
Q

what investigations would you do for someone suspected to have addisons?

A
  • U&Es: high k and low Na, raised urea
  • raised EST
  • FBC: normocytic normochromic anaemia
  • serum cortisol - should be low

ACTH (cosyntropin) stimulation test: measure cortisol before and after - failure to respond suggests primary insufficiency

adrenal autoAb - specifically against 21 hydroxylase

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120
Q

what is hyporeninaemic hypoaldosteronism?

A

low aldosterone due to low renin e.g. renal fualure.

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121
Q

How is primary hyperaldosteronism treated?

A

Depends on cause:

  1. Conns:
    • surgery - 1st line
    • spironolactone - used to correct K levels before surgery or if surgery is contraindicated
    • alternative to spironolactone is amiloride (K sparring)
  2. Bilateral adrenal hyperplasia:
    • amiloride
    • spironolactone
    • epleronone - new selective aldosterone antagonist (less side effects)
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122
Q

what does spironolactone do?

A

aldosterone receptor antagonist.
delayed response because blocks gene expression
less Na/K ATPase, Na/H, ENaC and ROMK
brings down BP by reducing Na and water reabsorption

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123
Q

what are the side effects of spironolactone?

A

impotence
gynacomasia
menstrual irregularity
GI effects

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124
Q

How do we treat cushings?

A

Depends on cause:

  1. drug induced –> stop medication
  2. adrenal adenoma –> unilateral adrenalectomy + steroid replacement post op (for 2yrs) due to chronic suppression of ACTH
  3. adrenal carcinoma: surgery however most have metastasised so radiotherapy or adrenolytic drugs
  4. bilateral adrenal hyperplasia: bilateral adrenalectomy and life long steroid and mineralocorticoid replacement
  5. Ectopic: surgery to remove tumour, block cortisol production meanwhile with ketonazole or metyrapone
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125
Q

what does etomidate and mifepristone do?

A

etomidate - blocks cortisol synthesis
mifepristone - blocks cortisol receptors

both can be used to treat cushings

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126
Q

how is adrenal insufficiency treated?

A

replace:
mineralocorticoids: flurdrocortisone once daily
glucocorticoids: hydrocortisone 3x a day - largest dose at A.M.
DHEA replacement

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127
Q

why is hydrocortisone used in addisons rather than prednisolone?

A

prednisolone has a longer half life and thus doesn’t mimic endogenous cortisol as well.

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128
Q

when treating someone for addisons, what monitoring may you do? How will you educate the patient?

A

monitor for glucocorticoid excess
take BP regularly and check U&Es

tell patient that during times of stress, exercise and operations the dose of steroids will need to be increased.

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129
Q

how does rifampicin affect steroid therapy?

A

increases clearance of cortisol and thus steroid dose needs to be increased in patients with addisons

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130
Q

what is an adrenal incidentaloma?

A

an incidental finding of an adrenal mass with no pathological significance. this is due to advances in imaging.
it is important to determine if they are malignant or benign

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131
Q

what are the differentials of incidentalomas?

A 
cortisol secreting adenoma - cushings
aldosterone secreting adenoma - conns
pheochromocytoma
carcinoma
metastasis 
androgen secreting adenoma
CAH 
cyst
Haematoma
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132
Q

what investigations would you carry out after finding an adrenal incidentaloma?

A

take a full history to find any symptoms associated with the mass
examination - look for signs of cushings etc
bloods: electrolytes and glucose
Blood pressure

urinary free cortisol and dexamethasone sup test

if BP is high and low K then look at aldosterone: renin ratio

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133
Q

how would you manage someone with an adrenal incidentaloma?

A

surgery if: hormone excess, pheochromocytoma, imaging suggests malignancy , more than 4cm

otherwise repeat MRI 6-12 months and annual biochemical screening

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134
Q

why is primary gonadal failure a.k.a. hypergonadotropic gonadal failure?

A

lack of oestrogen/testosterone leads to lack of negative feedback and gonadotrophs are hyperactive and thus LH and FSH are raised

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135
Q

what is seen in premature ovarian deficiency (primary gonadal failure)

A 
amenorrhea 
oestrogen deficiency - hot flushes, vaginal dryness, osteoporosis
raised gonadotrophins (LH, FSH especially)
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136
Q

what investigations would you do with a women presenting with premature ovarian deficiency?

A

low oestrogen
raised FSH, LH
karyotype for turners
look for autoAb

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137
Q

how would you manage primary ovarian insufficiency?

A

hormone replacement therapy

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138
Q

what are the causes of primary ovarian deficiency?

A

Chromosomal: Turners, Fragile X
genes: LH/FSH receptor dysfunction
autoimmune: lupus, T1D, addisons, myasthenia gravis, thyroid
chemo, radiotherapy, hystectomy

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139
Q

what is turners?

A

A chromosomal abnormality whereby females lack an X so have the genotype XO

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140
Q

what are the clinical characteristics of turners?

A 
short stature 
webbed neck
high arched palate
wide spaced nipples
low set ears 
down slating eyes 
gonadal dysgenesis --> amenorrhoea
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141
Q

what are the complications that are associated with turners?

A 
coarctation of the aorta
other heart defects 
hypothyroid 
osteoporosis 
coeliacs 
congential renal abnormalities
ENT problems
likely to be infertile
No mental problems
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142
Q

how can you diagnose turners?

A

karyotype lymphocytes

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143
Q

how do you manage turners syndrome?

A

early GH and sex hormone replacement
treat complications
baseline renal USS and thyroid autoAb regularly checked
3 yr ECHO

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144
Q

what is secondary gonadal failure?

A

failure of the gonads due to a problem in the pituitary/hypothalamus

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145
Q

what are the causes of secondary gonadal failure in women?

A 
PCOS
hypopituitarism
   - sheemans syndrome - necrosis of the pituitary secondary to hypovolaemic shock 
carpenter syndrome 
haemochromatosis, adenoma, trauma
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146
Q

what is PCOS?

A

a heterogenous genetic and hormonal condition characterised by hyperadrogenism, ovulatory dysfunction, hyperinsulinaemia and polycystic ovaries

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147
Q

what is the pathogenesis of PCOS?

A

GnRH impulses rise in frequency and amplitude
increase in LH and FSH
rise in LH stimulates androgens (high testosterone inparticular, but also oestrogen)
follicles are stimulated but none of them dominate –> cysts and amenorrhoea

high insulin also increases LH and also reduces SHBG and thus free levels of testosterone and oestrogen rise.

obesity, genetic predis and diabetes all contribute to the hyperinsulinaemia

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148
Q

what are the symptoms of PCOS?

A

hirsutism, deep voice, acne, irregular periods after an early menarche, male pattern baldness, obesity, often infertile

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149
Q

what is PCOS associated with?

A

Cancer - endometrial cancer and others
dyslipidaemia, T2D, insulin resistance and thus CVS risk.

reduced risk of osteoporosis

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150
Q

how do you diagnose PCOS?

A 
high testosterone, 
high LH/FSH ratio 
high prolactin
USS of ovaries - bilateral cysts
SHBG is low
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151
Q

How is PCOS managed?

A

weight loss - helps to improve insulin levels
metformin - help improve insulin sensitivity which will reduce LH and raise SHBG
OCP –> increase SHBG and inhibit LH release
GnRH analogs - supress LH/FSH secretion
Androgen receptor antagonist: spironolactone - contraindicated in pregnancy

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152
Q

what are the differentials for hyperandrogenic anovulation?

A 
CAH
androgen secreting tumour (of ovaries or adrenals) 
acromegaly
cushings
obesity induced
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153
Q

what symptoms would you get with androgen secreting tumours? when would you suspect this over PCOS?

A

high testosterone would cause hirsutism, virilisation, amenorrhoea.
suspect if testosterone is very high and there is rapid hirsutism/virilisation

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154
Q

women with PCOS can be given spironolactone. why is it important to combine with with OCP? what other monitoring needs to be done?

A

because spironolactone causes irregualar bleeding

monitor U&Es due to K+ sparring.

155
Q

how is primary gonadal failure in men characterised?

A

low testosterone but high LH/FSH

inability to produce adequate sperm

156
Q

what are the causes of primary gonadal failure in men?

A

klinefelters
XYY - tall and gonadal failure
congenital anorchia (HIV or autoimmune orchitis)
Noonan syndrome: normal karyotype and external genitalia however features of turners.

157
Q

how do men with primary gonadal failure present?

A

failure to progress through puberty
infertile
low libido, mood changes, lethargy

158
Q

what is klinefelters?

A

XXY genotype

159
Q

what are the clinical features of klinefelters?

A 
small firm testis. 
tall
long arm span 
reduced facial and pubic hair
gynacomastia 
cognitive dysfunction 
reduced libido
erectile dysfunction
160
Q

what are the complications associated with klinefelters?

A

CVS risk - due to high lipids (reduce risk with testosterone)
osteoporosis (reduce risk with testosterone)
DVT
T2D
breast cancer
autoimmune - lupus, sjogrens, RA

161
Q

how do you diagnose klinefelters?

A

karyotyping

162
Q

how do you treat klinefelters?

A

life long testosterone replacement therapy - improves strength, libido, osteoporosis, enlarges testis and facial hair

doesn’t effect fertility of gynacomastia

surgery for gynacomastia

163
Q

what are the causes of secondary gonadal failure in men?

A 
kallmann syndrome - GnRH deficiency and anosmia
ferile eunuch syndrome - incomplete GnRH deficiency 
idiopathic
anabolic steroids
drugs
haemochromatoiss
stress
pituitary adenoma
164
Q

how is secondary gonadal failure in men treated?

A

androgen replacement therapy

if fertility is desired stop ART and give gonadotrophins instead

165
Q

what is precocious puberty?

A

onset of puberty 2 sd’s below the mean. more common in girls
girls <8yrs
boys <9yrs

166
Q

what are the 2 categories of causes of precocious puberty?

A

gonadotrophin dependant (central) - excess LH/FSH

gonadotrophin independent (appearance of secondary characteristics due to hormones other than LH and FSH e.g. testosterone and oestrogen)

167
Q

what are the causes of gonadotrophin dependant precocious puberty?

A

gliomas, pineal tumours, HCG secreting germ cell tumours
CNS trauma
hydrocephalus

168
Q

what are the causes of gonadotrophin independent precocious puberty?

A

CAH
HCG secreting tumour of the liver
exogenous

169
Q

will precocious puberty make a person taller or smaller?

A

They will undergo growth spurt earlier and growth plates will close earlier and thus they will be short.

170
Q

how is delayed puberty defined?

A

initial changes are not present by 13/14 in G/B OR increased interval between start and finish

171
Q

what are the causes of delayed puberty?

A

turners
hypopituitarism
polyglandular autoimmune syndromes
post malignancy (chemo/radio)

172
Q

using FSH/LH levels how can you tell the cause of delayed puberty?

A

if high - primary cause: hypogonadism

if low - problem with pituitary

173
Q

what is hirsutism?

A

presence of excess hair growth in females due to increased androgens or increased sensitivity of the skin

174
Q

what are the causes of hirsutism?

A 
androgen secreting tumour
CAH
cushings 
PCOS
acromegaly

androgen independent: hypothyroid, phenytoin

175
Q

how can we treat hirsutism?

A

laser hair removal

eflornithine

176
Q

what is virulisation?

A

severe hirsutism : male pattern baldness, clitoromegaly and anabolic phenotype

177
Q

what is the difference between primary and secondary amenorrhoea?

A

primary - periods don’t start by age 16

secondary - periods stop >6 months

178
Q

what would you want to ask in the history of someone presenting with menstrual dysfunction?

A 
signs of oestrogen deficiency - hot flushes, vaginal dryness
age of mother/sisters period
duration of secondary amenorrhoea 
any family history of early menopause
check for anosmia - kallmans.
179
Q

what examination/investigations would you do on someone with menstrual dysfunction?

A 
BMI
pregnancy test
visual fields 
anosmia 
features of turners
LH, FSH and prolactin levels
180
Q

what could be the cause of menorrhagia? what is a complication of this?

A

heavy bleeding:

  • abnormal clotting
  • fibroids
  • copper coil

complication - anaemia

181
Q

what could be the cause of dysmenorrhoea

A

painful periods…

endometriosis, fibroids, coil, PID

182
Q

what are the causes of primary amenorrhoea?

A 
turners
CAH
Kallmans
LH/FSH receptor problems
imperforate hymen
pituitary disease
underweight/stress 
pcos
183
Q

what are the causes of secondary amenorrhoea?

A 
interuterine adhesions (ashermans syndrome)
hyperprolacinaemia 
PCOS 
haemochromatoiss of pituitary
thyroid dysfunction 
pregnancy, menopause
sheemans syndrome
184
Q

how does hyperprolactinaemia lead to amenorrhoea? what other complications does it have?

A

prolactin inhibits oestrogen.

galactorroea and blurred vision

185
Q

what can hyperprolactinaemia be caused by?

A 
pregnancy 
stress
anything reducing dopamine e.g. opiates
hypothyroid
adenoma
186
Q

if someone presents with amenorrhoea and high FSH what would be the diagnosis?

A

primary ovarian failure

karyotype for turners

187
Q

if someone presents with amenorrhoea and low LH/FSH what is the diagnosis?

A

pituitary problem

188
Q

if someone presents with amenorrhoea and has high prolactin what do you next rule out?

A

hypothyroid or pituitary adenoma

189
Q

how is menopause defined?

A

A period where there is no periods for 12 months around the age of 49 to 51. oestrogen levels fall and LH and FSH rise.

190
Q

list some of the effects of menopause

A

hot flushes, thinning of the cervix, vaginal dryness, urinary incontinence, osteoporosis (fractures), atherosclerosis risk increases

191
Q

what are the indications for hormone replacement therapy?

A

menopause
contraception
primary ovarian dysfunction

192
Q

what is used for emergency contraception? what is the side effects and what is important about this?

A

high dose of levonorgestrel within 72 hours of intercourse
can make you sick and vomit. it is important to warn patients to seek advice if this happens as the pill may no longer be effective

193
Q

what are the different methods of administration of the COCP?

A

monophasic - fixed O and P
biphasic - fixed O and P increases in second half
triphasic - fixed O and P increases in 2 stages

194
Q

how does the COCP work?

A

P and O inhibit LH/FSH secretion at anterior pituitary and thus inhibit development of follicle and ovulation
P and O lead to changes in the endometrium - atrophic and less accepting to implantation
P can cause cervical mucus to thicken

195
Q

what does the POP contain? how does this compare to COCP and why?

A

just progesterone
less reliable
because only acts by increasing cervical mucus thickness. has some effects on endometrium and ovulation but not as much as COCP

196
Q

how else can progesterone be given other than orally?

A

Transdermal, vaginal, nasal, injection, implant

MPA injection into buttocks every 12 weeks
etonogestrel I’mplant every 3 years

197
Q

state 5 bits of advice you would give to patients on OCP

A

if you miss a pill take it ASAP and if >12 hours then use another form of contraception for 7 days
if you vomit/ diarrhoea pill may not be effective
you will need 3 - 6 monthly BP checks
before you start we need to know about previous clots, strokes
some Abx can make the pill ineffective

198
Q

what are the ADRs of oestrogen?

A
  • breast enlargement and tenderness (for this reason slight increase in breast cancer)
  • nausea, vomiting, headaches
  • increased blood coagulation and increased risk of thromboembolism
  • reduced glucose tolerance and increased risk of IHD and stroke
    slight risk of endometrial cancer
    reduces labido
199
Q

what are the ADRs of progesterone?

A 
weight gain
acne
nausea and vomiting
headache
mood changes 
reduces labido

break through bleeding and increased risk of ectopic pregnancy - if POP

200
Q

what is oestrogen protective against?

A

ovarian cancer
improves acne
osteoporosis
improves heavy painful periods

201
Q

what are the contraindications to the COCP?

A 
migraines (indicator of stroke)
>35 and smoker
previous DVT/stroke
hypertension, diabetes , hyperlipidaemia
Fhx of breast cancer
thrombotic genetic disease
202
Q

how is HRT administered in menopause?

A

cyclic HRT is recommended when you start menopause - oestrogen for 25 days and then progestin between 10 and 14 days. 3-5 days no hormones

however also can do combined therapy - O and P everyday.

203
Q

how can the route of HRT in menopause vary?

A

depends on symptoms e.g. for hot flushes and osteoporosis take oral O and P
but for vaginal dryness can use topical vaginal gel.

204
Q

what are the contraindications of HRT in menopausal women?

A 
active breast or endometrial cancer
active DVT 
pregnancy 
undiagnosed vaginal bleeding 
history of DVT/PE, IHD, cerebrovascular disease
205
Q

what are the risks of HRT in menopausal women?

A

stroke, breast cancer, DVT, gall strones, endometrial cancer, mood changes, breast tenderness

206
Q

why is HRT given in premature ovarian insufficiency ?

A

women lack oestrogens so may have symptoms of oestrogen deficiency.
if hysterectomised can give P too for half the month to protect endometrium from hyperplasia
low dose androgens also improve fatigue and libido.

207
Q

when is androgen replacement therapy indicated?

A

for men with primary or secondary hypogonadism

208
Q

how does androgen replacement therapy help men?

A

improves strength, libido, tiredness, mood and secondary sexual characteristics
reduces risk of osteoporosis

209
Q

what are the ADRs of androgen replacement therapy?

A

adverse lipid profile
increased risk of atherosclerotic disease
risk of prostatic disease (check PSA regularly)
polycythaemia (increased RBC)

210
Q

what are the contraindications to androgen replacement therapy?

A

prostate or breast cancer (active)
benign prostatic hyperplasia
sleep apnoea

211
Q

where does the thyroid gland lie?

A

Its central isthmus lies just below the cricoid cartilage

212
Q

what is the structure of the thyroid gland ?

A

2 lobes covered in pretracheal fascia and connected by a central isthmus.
the fibrous septum divides the lobes up into psuedolobules which contain vesicles called follicles. follicles are lined by cuboidal epithelium.
follicles are filled with thyroglobulin

213
Q

which two nerves lie in close proximity to the thyroid and what is their role?

A

recurrent laryngeal
the external branch of the superior laryngeal

innervate the larynx for speech

214
Q

what vessels supply the thyroid gland?

A

superior, middle and inferior thyroid arteries/veins

215
Q

describe the production of T3/T4 by the thyroid

A
  1. Iodine is actively transported into the follicular cells.
  2. thyroglobulin is made by protein syn of tyrosine residues
  3. thyroid peroxidase iodinates the thyroglobulin to produce mono-iodothyronine (MIT) and di-iodothyronine
  4. the thyroglobulin is secreted into the lumen where MIT and DIT couple to produce T3 and T4 within the thyroglobulin
  5. There is endocytosis of thyroglobulin
  6. cleavage of thyroglobulin to release T3/T4
  7. exocytosis of T3/4
216
Q

how do T3 and T4 travel in the blood?

A

bound to TBG, Transthyretin (TTR) and albumin

217
Q

what is more potent T3 or T4?

A

T3 (also T4 is more bound to plasma proteins)

218
Q

how is thyroid hormone secretion controlled?

A
  1. stress and temperature act on the hypothalamus to stimulate TRH release
  2. TRH stimulates pituitary to release TSH (released in low amplitude pulses which are higher at night)
  3. TSH acts on the thyroid to stimulate T3 and T4 release. but also TSH leads to hyperplasia and increased vascularisation of thyroid cells
  4. free T3 and T4 can act via negative feedback on the hypothalamus and pituitary
  5. T4 is converted to T3 or inactive reverse T3 at peripheral tissues. both T3/4 are metabolised by the liver
219
Q

how do T3 and T4 act?

A
  • T3 and T4 are taken up by cells and acts on nuclear receptors to increase gene expression.
  • This leads to increased glucose uptake, increase B oxidation of fats and protein synthesis.
  • There is increased expression of receptors on heart and gut leading to increased HR and gut motility
  • The increased rate of protein synthesis requires more energy and thus increases the BMR.
  • The increased number of proteins in the cell means the cell is more active and thus increases BMR.
  • T3/4 is important for bone mineralisation and protein syn in heart and during development (myelination of nerves)
220
Q

what is meant by thyrotoxicosis? how does this differ from hyperthyroidism?

A

thyrotoxicosis is the clinical, physiological and biochemical findings when tissues are exposed to excess T3/4.
hyperthyroidism is the overactivity of the thyroid which leads to thyrotoxicosis

221
Q

what are the symptoms of hyperthyroid (general symptoms excluding graves specific symptoms)?

A

mental: hyperactive, irritable, insomnia
muscle: tired and weak
bowel: increased stool frequency
heart: increased HR, palpitations
temp: sweating and heat intolerance
lungs: dyspnoea
weight: weight loss despite increased appetite
urinary: thirst and polyuria
menstrual: oligo/amenorrhoea
skin: pruitis

222
Q

what are the signs associated with hyperthyroidism?

A

heart: tachycardia, cardiomegaly (shifted apex beat),
neuro: hyperrelexia, fine tremor , AF
skin: warm and moist , hair loss, palmar erythema
nails: onycholysis
periodic paralysis and psychosis (RARE)

osteoporosis (increased bone turnover)
T3/4 also lead to disruption of SHBG with oestrogen and thus free level of oestrogen rises - gynecomastia, reduced libido and erectile dysfunction.

223
Q

what are the additional symptoms associated with graves (other than hyperthyroid symptoms)?

A 
diffuse goitre
opthalmopathy: 
    - exophthalmos 
    - pain and discomfort
    - keratitis (due to exposure)
    - optic neuropathy
localised dermopathy - pretibial myxoedema 
thyroid acropachy 
lymphoid hyperplasia
224
Q

what allele and antigen is graves linked to?

A

antigen - CTLA -4

allele - HLA DR3

225
Q

what is graves disease?

A

autoimmune disease leading to hyperthyroid (most common type)
caused by autoAb to TSH receptor - thyroid stimulating immunoglobulins (TSI)

226
Q

who is graves disease more common in?

A

x5 more common in women

227
Q

what are the different causes of thyrotoxicosis ?

A

excess thyroid stimulation : graves, hashitoxicosis, pituitary adenoma, pituitary thyroid hormone resistance (excess TSH)

thyroid nodules: toxic solitary nodule or toxic multinodular goitre, thyroid cancer

inflammation: silent and post partum thyroiditis , subacute (de Quervain’s) thyroiditis, drug induced (amiodarone contains iodine)

exogenous hormones: levothyroxine or thyrotoxicosis facitita

high levels of hCG: pregnancy, choriocarcinoma (malignant tumour of trophoblastic cells, hydatidiform mole, testicular cancer. hCG has structural morphology with TSH

ectopic thyroid tissue : thyroid tumour mets, struma ovarii , teratoma containing functional thyroid tissue

228
Q

if a pituitary adenoma is resulting in thyrotoxicosis, what other clinical signs may there be to help in confirming it is a pituitary adenoma?

A

high T3/4 and TSH
visual changes and headaches
diffuse goitre

may cosecrete GH and prolactin

229
Q

what is thyrotoxicosis facitita? what would you see clinically, biochemically and on imaging?

A

ingestion of exogenous thyroid hormone (not levothyroxine)
no thyroid enlargement
increased T4 but supressed TSH
low thyroglobulin - differentiates it from thyroiditis
depressed thyroid uptake on scintigraph

230
Q

how can a struma ovarii lead to thyrotoxicosis?

what is seen clinically and on imaging

A

ovarian teratomas can contain hyperfunctioning thyroid tissue.
no thyroid enlargement
depressed thyroid uptake on scintigraphy

231
Q

how can you confirm diagnosis of struma ovarii causing thyrotoxicosis?

A

Body scan after radioactive iodine

232
Q

what is thyroid crisis/storm?

A

A complication of thyrotoxicosis where there is a excessive release of thyroid hormones leading to a hypermetabolic state. rare but life threatening.

233
Q

what are the clinical signs suggestive of thyroid storm ?

A

severe signs of hyperthyroid:

  • severe tachycardia and arrhythmias
  • fever
  • altered mental status, delirium, seizure
  • vomiting, jaundice and diarrhoea

eventually cardiac failure, respiratory failure, renal failure, hepatomegaly and dehydration

234
Q

what haematological finding may you find during a thyroid storm?

A

raised T3/4
leucocytosis
raised ALP
hypercalcaemia

235
Q

what conditions are associated with graves?

A 
T1D 
addisons
pernicious anaemia
virtiligo 
alopecia areata 
myasthenia gravis 
coeliacs 
anything associated with HLA DR3
236
Q

what causes thyroid crisis/storm ?

A

poorly controlled hyperthyroid with complicating acute infection, surgery or radioactive iodine therapy

radioactive iodine kills thyroid cells and thus releases T3/4

other drugs: NSAIDs, chemo, excessive thyroxine medication

diabetic ketoacidosis

237
Q

how is thyroid crisis/storm treated?

A

need to identify and treat quickly and aggressively or could quickly lead to death.

supportive:

  • digoxin (for arrhythmias), fluid and cooling
  • B blockers/Ca channel blockers

specific:

  • antithyroid drugs in large doses: propylthiouracil or methimazole
  • potassium iodine drops after starting antithyroid drugs (inhibits thyroid hormone release)
  • glucocorticoids (prednisolone) in high doses preventing convertion of T4 to T3
  • may need dialysis to remove excess T3/4
238
Q

what is subclinical hyperthyroid ?

A

TSH is low but T3/4 are normal and there may be subtle signs of thyrotoxicosis

239
Q

what could cause subclinical hyperthyroidism?

A

may be caused by underlying graves or exogenous levothyroxine in treatment of hypothyroid

240
Q

do we need to treat subclinical hyperthyroidism?

A

no but repeat TFTs every 6 months
if AF or osteoporosis then radioactive iodine is considered
if cause is exogenous reduce dose of levothyroxine

241
Q

what is thyrotoxic periodic paralysis? what biochemical chnges are seen during this?

A

complication of thyrotoxicosis whereby there is painless muscle weakness for minutes to days.
this is accompanied by flaccid paralysis and hyporeflexia that spreads proximally to distally

low serum K 
Creatine phosphokinase (CPK) rises during the recovery phase
242
Q

what precipitates thyrotoxic periodic paralysis?

A

insulin, carbohydrate and vigorous exercise

243
Q

how is thyrotoxic periodic paralysis treated?

A

K replacement

treat thyrotoxicosis

244
Q

how is thyrotoxicosis and pregnancy linked?

A

thyrotoxicosis can occur during pregnancy - gestational thyrotoxicosis
similar signs to normal thyrotoxicosis.

245
Q

what are the maternal complications of uncontrolled hyperthyroidism in pregnancy?

A 
preg induced hypertension
preterm delivery
congestive heart failure 
thyroid storm 
miscarriage 
haemorrhage
246
Q

what are the foetal complications of uncontrolled hyperthyroidism in pregnancy?

A 
hyperthyroidism
neonatal hyperthyroidism 
intrauterine growth retardation 
small for gestational age
prematurity 
still birth 
cranial stenosis
247
Q

what is thyroid hormone resistance?

A

syndrome characterised by reduced responsiveness to free T3/4 levels and normal or elevated TSH

due to mutation in thyroid hormone receptor.

248
Q

how does thyroid hormone resistance present?

A

usually goitre is he only clinical feature present
but may be short stature, hyperactive, attention deficits and learning difficulties.
usually found accidently on routine check up

249
Q

do you need to treat thyroid hormone resistance?

A

usually no

250
Q

what is the most common form of hypothyroidism and how is it caused?

A

Hashimotos

auto Ab to TSH receptor that block the receptor

251
Q

what are the clinical symptoms of hypothyroidism?

A 
weight gain and loss of appeptite
constipation 
bradycardia
cold intolerance 
tirednesss
muscle stiffness, cramps and carpal tunnel
menorrhagia 
dry skin and hair loss 
deep hoarse voice 
depression 
reduced visual acuity
252
Q

what is a myxedema coma and what is it triggered by triggered by?

A

respiratory depression and increased CO2. also see hyponatraemia, impaired water excretion and disorder of ADH excretion

predisposed by cold exposure, trauma, infection and CNS depressants

253
Q

what are the non-goitrous causes of hypothyroidism?

A

thyroidectomy
radioiodine
congenital developmental defect
hypopituitarism or hypothalamic neoplasm/sarcoidosis/infection

254
Q

what are the clinical features of myxoedema in hypothyroid?

A 
dull expressionless face
periorbital oedema - buzz word 
macroglossia 
sparse hair 
pale, cool skin that feels rough and doughy 
megacolon and intestinal obstruction 
enlarged heart
neuro: encephalopathy and peripheral neuropathy , ataxia, psychosis and depression

pretibial myxoedema - puffy skin over tibia - also seen in graves.

255
Q

what is myxoedema?

A

Term used synonymously with severe hypothyroidism. However, the term is also used to describe a dermatological change that can occur in hypothyroidism and some forms of hyperthyroidism.

in severe hypothyroid there is accumulation of hydrophilic mucopolysaccharides in the ground substance of the dermis leading to thickening of facial features and doughy skin

256
Q

what are the goitrous causes of hypothyroidism?

A 
iodine deficiency
drug induced (amiodarine, iodines, some antiretrovirals)
257
Q

what are the causes of congenital hypothyroidism?

A

thyroid agenesis

thyroid hormone dysgenesis (abnormal metabolism and production of T3/4)

258
Q

what are the clinical features of congenital hypothyroidism?

A 
jaundice
goitre
hoarse cry 
feeding problems
constipation 
short stature
delay in develop 
dry skin and sparse hair. 
slow relaxing reflexes - buzz word
259
Q

why is early treatment essential in congenital hypothyroidism?

A

prevent cerebral damage

260
Q

what is subclinical hypothyroidism?

A

normal T3/T4 but high TSH

261
Q

what is a goitre?

A

enlarged thyroid
may accompanying hypothyroid, hyperthyroid
some are euthyroid.

most goitres are benign

262
Q

how can we classify goitres?

A

uninodular - one thyroid nodule
multinodular - can be active or inactive
diffuse - whole thyroid enlarged due to hyperplasia

263
Q

list the different causes of goitres

A

Iodine deficiency - most common cause world wide
Hashimotos - diffuse
Graves - diffuse pattern
pituitary adenoma - hypersecretion TSH - diffuse pattern
thyroid hormone resistance
thyroiditis
thyroid cancer
congenital hypothyroid - in born errors of thyroid hormone synthesis
drug induced - amiodarone, lithium, antithyroid

264
Q

why does iodine deficiency lead to a goitre? how can this be treated?

A

The thyroid gland enlarges to compensate for the deficiency. gives a diffuse growth pattern
treated with iodine

265
Q

what is thyroiditis? what is it caused by?

A

hyperthyroid initially but then progresses to hypothyroid

caused by:

  • hashimotos: chronic lymphocytic infiltration
  • postpartrum
  • Radiation
  • De Quervains
  • durg induced - amiodarone
  • pyogenic: S.aureus, Streptococcus, Ecoli, fungi, TB
  • Riedel’s thyroiditis
266
Q

what is Riedel thyroiditis? how do we treat this?

A

rare disorder of intense fibrosis of thyroid gland and nearby structures (salivary and parathyroid gland)
patients usually euthyroid

treated with corticosteroids.

267
Q

what type of goitre does thyroid cancer normally present as?

A

usually uninodular

however thyroid microcarcinomas can be found in multinodular goitres

268
Q

when is a thyroid cancer suspected?

A

rapidly enlarging goitre
age 20-60 esp 40-50
dysphagia, stridor, hoarseness
family history

269
Q

what type of cells do the majority of thyroid cancers originate from? is the prognosis of these good or bad? how are they treated?

A

papillary cancers - from papillary cells
good prognosis
can be treated by thyroidectomy, post op TSH suppression followed by levothyroxine

270
Q

what would the basal thyroid function tests be in primary hyperthyroidism/hypothyroidism, secondary hyperthyroidism/hypothyroidism and thyroid hormone resistance?

A

primary hyperthyroidism: high T3/4, low TSH
primary hypothyroidism: low T3/4, high TSH
Secondary hyperthyroidism: high T3/4 and TSH
Secondary hypothyroidism: low T3/4 and TSH
thyroid hormone resistance: all high

271
Q

what are the possible causes of supressed TSH and normal free T3/4

A

subclinical thyrotoxicosis
recovery from thyrotoxicosis
excessive thyroxine replacement
sick euthyroidism

272
Q

what is the cause of high T4 and normal T3 and TSH

A

amiodarone

273
Q

what is the cause of high T3 but normal T4/TSH

A

T3 thyrotoxicosis

274
Q

what states can increase thyroid binding globulin - TBG?

A 
pregnancy
new born
OCP
tamoxifen
hep A
275
Q

what states can decrease (thyroid binding globulin) TBG?

A 
androgens, 
glucocorticoids e.g.. in cushings 
chronic liver disease
acromegaly
nephrotic syndrome
phenytoin
276
Q

what drugs can increase the clearance of thyroid hormones?

A

phenytoin and carbamazepine and thus will disrupt TFTs

277
Q

what drugs increase and decrease TSH secretion

A

Increase:
- amiodarone, sertraline, st johns wort
decrease:
- glucocorticoids, phenytoin, dopamine

278
Q

what drug alters T4 synthesis?

A

increased by iodine

decreased by iodine and lithium

279
Q

what drugs inhibit T4 binding to TBG?

A

salicylates

furosemide

280
Q

what investigations can we do for a patient with suspected thyroid problem?

A 
TFT
antibody screening
scintiscanning 
ultrasound scanning
fine needle aspiration 
CT scan - can look at structures around thyroid e.g. great vessels/trachea being supressed
281
Q

how can antibody screening help diagnosis of thyroid problems? What else can such screens be useful for?

A

antithyroid peroxidase (anti TPO) Ab or antithyroglobulin Ab are found in patients with autoimmune disease (hashimotos and graves)

high risk individuals can also be screened for these Ab to test their risk of developing thyroid problems e.g. T1D, AF and hyperlipidaemia

TSH receptor Ab can also be tested for

282
Q

what is the scintiscanning test for?

A

localises sites of radiation for areas of hyper or hypo acitivity. this allows us to differentiate between different types of disease

e.g. Graves - enlarged gland with intense and homogenous radioactive uptake
thyroiditis - low/absent uptake
toxic nodule - one area of intense uptake

283
Q

what is the use of USS of the thyroid?

A

thyroid size
differentiates cystic nodules from solid ones
can differentiate benign and malignant

284
Q

on USS of the thyroid what is suggestive of malignany?

A

microcalcifications (prominent feature of medullary carcinoma of the thyroid)
irregular nodules

285
Q

how does CT scanning help in thyroid disease?

A

can look at structures around - e.g. if trachea and great vessles are being compressed
can look to see if malignancy is infiltrating adjacent structures e.g. carotid artery, IJV, trachea, oesophagus

286
Q

other than deranged TFTs what other abnormalities can be found in blood tests in thyrotoxicosis? in hypothyroid?

A

Thyrotoxicosis:

  • normocytic anaemia
  • neutropenia
  • ALP raised
  • mild hypercalcaemia
    hypothyroid:
  • CK may be raised and raised LDL
  • prolactin may be raised due to raised TRH
287
Q

what are the 3 main categories of treatment of hyperthyroid?

A

Drug therapy
radioactive iodine
surgery (partial thyroidectomy)

288
Q

what are the different drug therapies for hyperthyroidism?

A

B blockers - symptom control
antithyroid drugs:
- carbimazole - inhibits thyroid peroxidase
- propylthiouracil - inhibits thyroid peroxidase and the conversion of T4 to T3

289
Q

what are the ADRs of antithyroid drugs?

A 
GI symptoms
change in smell and taste
agranulocytosis (reduced granulocytes) - very rare but potentially fatal - increased risk of infection 
allergies - rash
transient leucopenia 
alopecia
maculopapular rash 
cholestatic jaundice - abnorm LFTs (rare again)

generally well tolerated

290
Q

how long does carbimazole take to show effect?

A

months to have effect

291
Q

how often is carbimazole taken and how is it metabolised?

A

once dialy
converted by liver to active metabolite - methimazole
excreted by kidneys

292
Q

what advice would you give a patient who is about to start carbimazole?

A

warn patient if there is any events of fever or severe sore throat tell them to stop taking medication and seek medical attention immediately. This is incase of agranulocytosis (a rare side effect)

293
Q

what are the contraindications of antithyroid drugs e.g. carbimazole?

A

hypersensitivity
impaired liver
previous haematological issue
breast feeding

294
Q

what are the DDI of carbimazole?

A

before starting carbimazole the patient will be in a state of hyperthyroid and thus metabolism of drugs will be faster e.g. warfarin.
So once carbimazole is started the metabolism will be reduced and so medication doses need to be adjusted.

295
Q

what are the two different drug regimes in hyperthyroidism?

A

dose titration regime:
- aim to achieve euthyroid with a high dose and then slowly reduce to maintain it with the lowest possible dose (titrated according to TFTs)

block and replace regime:

  • carbimazole to block the thyroid and then replace the losses with levothyroixine. this avoids iatrogenic hypothyroidism.
  • after 12-24 months the size of the thyroid may have reduced, in which case the drugs can slowly be stopped
296
Q

what are the indications of radioactive iodine for hyperthyroidism? what are the contraindications?

A

relapsed graves disease
definitive treatment for multinodular goitre of adenoma

contraindications:

  • young children - risk of malignancy
  • pregnant/lactating women
297
Q

how does radioactive iodine therapy help treat hyperthyroid?

A

only thyroid will uptake the iodine and thus the radioactivity will kill thyroid cells and reduce thyroid hormone synthesis.
response is slow

298
Q

what are the side effects of radioactive iodine therapy?

A

rare: anterior neck pain caused by radiation induced thyroiditis
transient rise in plasma T4 in first 2 weeks after therapy (killed cells release contents)
hypothyroidism

299
Q

what guidance would you give patient undergoing radioactive iodine therapy?

A

stop anti thyroid drugs 7 days before.

300
Q

what occurs in a partial thyroidectomy? when is this indicated?

A

Continue antithyroid drugs until day of surgery
Thyroid gland is partially removed. some thyroid and parathyroid gland is left behind
potassium iodine drops post op period for 7-10 days to reduce vascularity of gland

indicated in those with large multinodular goitre or those intolerant to drug therapy

301
Q

what is a common side effect amongst thyroidectomy and radioiodine therapy?

A

hypothyroidism

need to give levothyroxine

302
Q

what are the complications of thyroidectomy?

A

immediate:

  • recurrent laryngeal nerve damage
  • hypoparathyroidism
  • thyroid crisis
  • local haemorrhage (causing laryngeal oedema)
  • wound infection

later:

  • hypothyroid
  • keloid formation
303
Q

How can we treat hypothyroidism?

A

levothyroxine (T4):

  • young patients - start at 50mg - 100mg and can reach up to 100-200 mg /day by going up in 25mg
  • in elderly with history of IHD start at 25mg-50mg and then increase 25mg at 4 week intervals

dose requirements increase during pregnancy
note some conditions may affect absorption: coeliacs, phenytoin, omeprazole, rifampicin and H.pylori

304
Q

what monitoring is important for someone on levothyroxine ?

A

TFTs on an annual basis

305
Q

what are the common side effects of levothyroxine?

A

anxiety, weight loss, insomnia, diarrhoea, menstrual irregularities

306
Q

when can the dose of levothyroxine be reduced?

A

new onset AF, angina or cardiac failure
accelerated bone loss
high T3

all suggestive of subclincal hyperthyroid or hyperthyroidism

307
Q

how can we treat myxoedema?

A

IV levothyroxine - start with loading dose and then lower the dose.

308
Q

what is sick euthyroid syndrome?

A

low T3/4 and low/normal TSH
tissue thyroid hormones are low

this is secondary to severe illness (end stage malignancy, liver failure, renal failure, severe infection)

thyroxine replacement is not indicated - no evidence its good.

309
Q

in history of thyroid disease what should you ask about other medical conditions?

A

evidence of other autoimmune disease

310
Q

how does hyperthyroidism affect bone health in children and adults?

A

children: accelerated skeletal maturation and advanced bone age.
adults: generalised osteoporosis leading to vertebral fractures and kyphosis

311
Q

how does hypothyroidism affect bones in children and adults?

A

children: delayed physeal closure and bone age in infants (also retardation and tiredness). absent epiphysis and associated with slipped capital femoral epiphysis
adults: generalised osteoporosis , soft tissue oedema and carpal tunnel.

312
Q

how is acromegaly linked to bone and joint health?

A

carpal tunnel
premature osteoarthritis
degenerative disc disease
osteoporosis

313
Q

Describe the difference between primary, secondary, tertiary and malignant hyperparathyroidism

state some causes of each.

A

primary: gland failure - excess PTH and thus Ca rises and PO4 drops. caused by adenoma (majority), hyperplasia or parathyroid cancer.
secondary: low Ca and thus high PTH (physiologically normal response). Occurs due to renal failure or low Vit D intake
tertiary: prolonged secondary and thus eventually the parathyroid gland becomes hyperplastic and produces excess PTH and now Ca starts to rise.
malignant: PTH related protein (PTHrP) is secreted by small cell lung cancer, breast and renal cell carcinomas.

314
Q

What changes are seen in Ca, PO4, ALP and PTH in different types of hyperparathyroidism

A

primary: high PTH, High Ca and low PO4 , high ALP
- also can be seen in tertiary, thiazides and lithium
secondary: high PTH, low Ca
tertiary: high PTH, normal/high Ca

315
Q

what Xray changes are seen in hyperparathyroidism?

A

generalised osteopenia
bone scleorosis
brown tumours
bone resorption

primary: chondrocalcinosis (knee, wrist, pubic symphysis)
secondary: rugger jursey spine, bone sclerosis and soft tissue calcification.

316
Q

how can we treat hyperparathyroidism?

A

diet: restrict Ca or increase Ca depending on cause. keep hydrated (protect from stones)
surgery : if calcium is very high, renal stone, bone disease then can remove adenoma
cinacalcet - increases sensitivity of parathyroid to ca and thus reduces PTH

317
Q

what are the side effects of cinacalcet ?

A

myalgia

reduced testosterone

318
Q

what are the risks of removing the parathyroid gland?

A

hypoparathyroidism

recurrent laryngeal nerve palsy (hoarseness of voice)

319
Q

what is the normal regulation and physiology of PTH, vitamin D and calcitonin?

A

PTH is a polypeptide hormone. normally Ca binds GPCR on chief cells to inhibit the release of PTH. Therefore reduced Ca, high PO4 and high Mg all stimulate PTH release

PTH inhibits osteoblasts and promotes osteoclasts, increases renal Ca reabsorption and activates Vit D

Vit D increases Ca absorption from gut and inhibits bone resorption

overall Ca rises in serum and PO4 decreases

calcitonin does the opposite and lowers serum ca

320
Q

what is the difference between primary, secondary and pseudo and pseudopseudo - hypothyroidism?

state some causes of each

A

primary: problem with parathyroid at producing PTH (low Ca and high PO4) e.g. congential (DiGeorge) or autoimmune.

secondary to surgery (thyroidectomy, parathyroidectomy), radiation and low Mg

pseudohypoparathyroidism: failure of target gland to respond to PTH - genetic cause

pseudopseudohypoparathyroidism - same clinical features and pseudo however normal biochemistry. genetic cause.

321
Q

what blood results would you expect in the different forms of hypoparathyroidism?

A

primary and secondary: low Ca, low PTH , and high PO4

pseudo: high PTH, low Ca

pseudopseudo - normal

322
Q

what do you find on clinical examination of someone with pseudohypoparathyroidism

A 
short stature
round face
short metacarpals
neuromuscular problems
GI problems.

(see this on pseudopseudo as well)

323
Q

what symptoms would you get with primary or secondary hypoparathyroidism?

A

hypocalcaemia symptoms

324
Q

what Xray changes would you see in hypoparathyroidism?

A

sclerosis
calcification of subcutaneous tissue
basal ganglia calcification in pseudohypoparathyroid

325
Q

what is the treatment for hypoparathyroidism?

A

calcium supplements

in primary can also give PTH analogs and calcitriol

326
Q

how does function of PTHrP compare to PTH?

A

doesn’t affect vitD activation and thus less protective against bone health

327
Q

what are the causes of hypercalcaemia?

A

Common:

  • -hyperparathyroidism
  • -malignancy - PTHrP, bone mets (prostate and breast), myeloma
  • thyrotoxicosis - increased osteoclast activity as well as hyperadrenerfic state

less common:

  • vit D intoxication
  • sarcoidosis
  • familial hypercalciuric hypercalcaemia

uncommon
- thiazides, litheium, addisons, renal failure
(also granulomatous conditions)

328
Q

what are the symptoms of hypercalcaemia?

A
  • tired, depressed, weak
  • thirsty, dehydrated, polyuria
  • renal stones
  • abdo pain, constpipation
  • pancreatitis, ulcers
  • pain
  • factures - osteopenia
  • increased BP
  • ECG - decreased QT

moans groans and stones

abdo pain, vomiting and coma when it gets very high.

329
Q

someone with hypercalcaemia has:

  • high ALP, low PO4
  • high ALP, high PO4
  • normal ALP, high phosphate

what are the differentials?

A

high ALP, low PO4 –> hyperparathyroidism
high ALP, high PO4 –> bone mets, thyrotoxicosis, sarcoidosis

normal ALP, high PO4 –> excess Vit D, myeloma

raised albumin and urea too –> dehyrdration

330
Q

how do you manage mild hypercalcaemia?

A

avoid thiazides
increase hydration (avoid stones)
reduce VitD/Ca from diet
review 6 monthly

check for complications:

  • bone health: Xray and DXA
  • ECG
  • renal USS for stones

may want to give bisphosphonates to protect bone if cause is exces breakdown.

331
Q

how do you manage acute/emergency hypercalcaemia?

A

give large amounts of IV 0.9% saline to dilure/rehydrate

loop diuretic - may be given
dialysis may be needed if severe

bisphosphonates to protect bone

treat cause e.g. parathyroidectomy

332
Q

what are the causes of hypocalcaemia?

A 
hypoparathyroidism
failure to activate VitD 
    - deficiency
    - renal failure - e.g. acute rhabdomyosis
    - pancreatitis
    - drugs ketonazole
hypocalacemic drugs:
   - cisplatin, calcitonin, bisphosphonates and oral phosphate
respiratory alkalosis
333
Q

what are the symptoms of hypocalcaemia?

A

SPASMODS

  • Spasm/cramps
  • paraesthesia
  • anxiety
  • Seizures
  • muscle tone increased
  • orientation impaired
  • dermatitis
  • stridor (laryngospasm)
334
Q

what are the two signs of hypocalcaemia?

A

Chvostek’s sign: facial nerve gets traped infront of ear and causes corner of mouth to twitch

Trousseau’s sign: inflation of BP cuff causes flexion of wrist and fingers

335
Q

what investigations could you carry out if you suspect hypocalcaemia?

A

serum Ca, PTH and 1,25 vit D levels

skull radiograph in chronic cases will show calcification of basal ganglia

336
Q

how can you treat acute symptomatic hypocalcaemia?

A

IV calcium gluconate infusion to help bring Ca back up. keep monitoring calcium levels.

also important to monitor cardiac rhythm throughout esp in heart disease and those on digoxin, because sudden changes to calcium can result in arrhythmias

if not responding, consider hypoMg being a cause and thus Mg infusion

337
Q

how will an acute symptomatic case of hypocalcaemia present?

A

tetany and seizures

338
Q

how do you treat hypocalcaemia due to hypoparathyroidism

A

give Ca supplements such that patient is asymptomatic.
should not aim to give ca to reach normal levels because this will increase risk of stone formation (there is no PTH to promote reabsorption so calciuria)

339
Q

how do you generally treat chronic hypocalcaemia

A

adequate Ca and vit D in diet

340
Q

what is osteomalacia?

A

softening of bones due to abnormal mineralisation. can be due to inadequate PO4, Ca and VitD

341
Q

what are the causes of osteomalacia?

A

mainly dietary, lack of sunlight
tumour induced
drug induced: glucocorticoids and phenytoin
chronic renal failure

342
Q

how will someone present with osteomalacia?

A

weak, malaise , tired, muscle pain , bone pain
recurrent fractures

on examination may be weaker and have a waddling gait.

343
Q

what XRAY changes are seen in osteomalacia?

A

osteopenia

loser zones

344
Q

how is osteomalacia managed?

A

vit D supplements
bone protection
advice to get sunlight.

345
Q

what blood results are seen in osteomalacia…

A

low ca, vit D, phosphate

high PTH and ALP

346
Q

what is Rickets?

A

abnormal bone metabolism seen in children due to deficiency of Ca and PO4 most commonly due to vit D deficiency and thus malabsorption

some are inherited forms of rickets but mainly due to poor nutrition

osteoid is made but cant mineralise properly and thus not strong so physeal plates become distorted when weight is beared on them. leads to deformity.

347
Q

what is the presentation of rickets?

A 
bone pain and deformity
tetany
seizures
rachitic Rosay
Genovarum 
frontal bossing 
slipped capital femoral epiphysis
348
Q

what is seen on XRAY of someone with rickets?

A

prominent epiphysis due to excessive not ossified tissue

349
Q

what are the biochemical findings of someone with rickets?

A

low Ca, VitD, po4

high ALP and PTH

350
Q

how do we treat rickets?

A

give Vit D and calcium supplements generally

if renal failure - active form of vit D is needed

if hypophosphataemic rickets - PO4 supplements and active Vit D. monitor ALP throughout treatment.

351
Q

what are the causes of obesity?

A

single gene - rare:
- leptin deficiency
- prader willi syndrome
environmental: increased intake and reduced exercise
secondary cause: cushings, hypothyroidism

352
Q

how is obesity diagnosed?

A

BMI = weight (Kg)/ height(m) squared

<18.5 underweight
18.5-24.9 = normal
25-29.9 = overweight 
30-34.9 = obese
35 + = severly obese
353
Q

how should we evaluate someone with obesity?

A

weight history from birth
previous treatments and success’s
comorbidities
smoking, alcohol, diet and eating triggers
look for xantoma, skin tags and hyperpigmentation on neck
other symptoms to consider secondary causes

354
Q

how can we treat obesity?

A

diet and exercise
drug therapy: orlistat and phentermine
surgery - bariatric surgery improves for 8yrs

355
Q

what is orlistat? contraindications?

A

intestinal pancreatic lipase inhibitor
reduces fat absorption

contraindicated in cholestasis and malabsorption syndromes

consider giving vit D supplements if worried about fat vit absorption

356
Q

what is phentermine? cautions?

A

NA/Dopamine release inhibitor - reduces appetite

caution in hypertension and vascular disease

357
Q

what is metabolic syndrome?

A

cluster of factors: hyperinsulinaemia, glucose intolerance/diabetes, obesity, hypertension, hyperlipidaemia.
associated with increased risk of CVS disease

358
Q

what are clinical signs of insulin resistance

A

skin tags and hyperpigmentation of neck

359
Q

how is hypoglycaemia defined?

A

when glucose levels <3mM associated with symptoms of neuroglycopenia and reversal of symptoms with correction of glucose.

360
Q

what are the causes of hypoglycaemia?

A

excessive insulin (most common):

  • antidiabetic drugs - oral hypoglycaemic, insulin
  • alcohol
  • insulinoma

impaired endocrine response:

  • addisons - GH deficiency
  • Excess IGF1 (tumour)

impaired hepatic glucose metabolism

- liver failure
- Hepatocellular carcinoma

other:
- infection : sepsis or malaria
- starvation/anorexia
- glycogen storage disease
- post prandial reactive hypo

361
Q

what is a non-islet cell tumour hypoglycaemia?

A

excess IGF1 from tumours such as fibrosarcomas and mesotheliomas. lead to reduced glucose, insulin and GH.
remove tumour. but before surgery available treat with high dose corticosteroids

362
Q

what is post prandial reactive hypoglycaemia?

A

occurs after a meal due to a miss match in glucose being taken up by cells and entering the circulation

363
Q

what investigations could be carried out in some one who is thought to be hypoglycaemic

A

glucose plasma levels checked
U&Es, LFTs,
fasting glucose and C peptide - if high insulinoma
cortisol test

364
Q

when is IM glucagon not affective in hypoglycaemia?

A

if hepatic function is impaired

contraindicated if known insulinoma - may stimulate further insulin release

365
Q

how is chronic hypoglycaemia treated?

A

chronic hypo may be due to excess insulin release

can be treated with diazoxide - inhibits insulin from pancreas

366
Q

what are multiple endocrine neoplasias (MEN)?

A

group of syndromes featuring tumours of endocrine glands

367
Q

what is MEN1

A

autosomal dominant. mutation in tumour suppressor gene
leads to parathyroid tumour, anterior pituitary adenoma and pancreatic tumours.
for clinical diagnosis you need 2/3 of above or 1/3 and family history

368
Q

what pituitary tumours may occur in MEN1

A

cushings
acromegaly
prolactinoma
nonfunctioning

369
Q

what pancreatic tumours may occur in MEN1

A

gastinoma
insulinoma
glucagonoma
non functioning

370
Q

other than parathyroid tumours, pancreatic and pituitary tumours what other tumours may be associated with MEN1

A 
carcinoid
cortical adrenal gland 
pheochromocytoma
lipoma 
malignant melanoma
371
Q

what is the most common presenting complaint in MEN1

A

symptoms of hyperparathyroidism

372
Q

how can we manage MEN1

A

parathyroid tumour: total parathyroidectomy is recommended because of reoccurance

pituitary adenoma: TSS and medical therapys and radiation

pancreatic: remove pancreas (PPIs for gastrinoma)

screen family members

373
Q

what is MEN type 2 caused by and what 3 groups can it be split into?

A

autosomal dominant condition. protooncogene C-RET

MEN2a, 2b and FMTC

374
Q

what is MEN 2a characterised by?

A

familial medullary thyroid carcinoma (FMTC)
pheochromocytoma
parathyroid tumour

most common

375
Q

what is MEN2b characterised by?

A

familial medullary thyroid carcinoma (FMTC)
pheochromocytoma
mucosal neuroma
marfanoid habitus

376
Q

what is MEN FMTC characterised by?

A

familial medullary thyroid carcinoma (FMTC) alone

377
Q

what do familial medullary thyroid carcinoma (FMTC) resemble

A

C cells ad secrete calcitonin

but rarely lead to hypocalcaemia

378
Q

how is MEN type 2 managed

A

FMTC - thyroidectomy followed by levothyroxine
pheochromocytoma: A and B blockade, surgical resection
screen relatives:
- urinary catecholamine
- calcium
- calcitonin levels

379
Q

A lady has hypothyroid and high LDLs how would you treat this?

A

Hypothyroid can result in high LDLs

If the thyroid problem is treated the LDLs will resolve and thus give thyroxine and no need for statins

380
Q

how is being overweight linked to amenorrhoea?

A

overweight and insulin resistance is linked to PCOS

PCOS is most common endocrine problem in females

381
Q

why is subclinical hypothyroid a problem in pregnancy?

A

high TSH is linked to low QI

therefore subclinical hypothyroid is treated with levothyroxine in pregnancy so that this will lower TSH

382
Q

is subclinical hypothyroid treated?

A

yes in pregnancy
not usually otherwise
- in those with subclin hypothyroid do a Hashimotos Ab test - if positive then 20% chance of developing hypothyroid and therefore monitor them regularly. however if Ab test is negative they are unlikely to and thus can be discharged.

if TSH is very high may give a low dose of levothyroxine

383
Q

what are thyroid peroxidase (TPO) Ab associated with?

A

hypothyroid - hashimotos

General Medicine sara (4 decks)

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